Ask about this productRelated genes to: NEGR1 antibody
- Gene:
- NEGR1 NIH gene
- Name:
- neuronal growth regulator 1
- Previous symbol:
- -
- Synonyms:
- KILON, MGC46680, Ntra, IGLON4
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-09
- Date modifiied:
- 2014-11-19
Related products to: NEGR1 antibody
Related articles to: NEGR1 antibody
- Traumatic brain injury (TBI) can cause severe neurological damage. Ferroptosis, a recently discovered form of iron-regulated cell death, is closely associated with TBI. Cannabidiol (CBD) has been demonstrated to exhibit neuroprotective effects. However, the antiferroptotic role of CBD in TBI remains unclear. Investigating whether CBD inhibits ferroptosis after brain injury and its underlying mechanisms is of great significance. We find that ferroptosis can be induced in rats after TBI, and CBD significantly inhibits ferroptosis in TBI rats both and . MicroRNAs (miRNAs) are highly expressed in the brain. Differentially expressed miRNAs and mRNAs after TBI are detected by RNA sequencing, and miR-320-3p, Negr1, and the ERK/MEK pathway are screened out due to their strong correlations. The results show that CBD inhibits miR-320-3p expression, increases Negr1 expression, and suppresses the ERK/MEK pathway both and . Mechanistically, transfection with miR-320-3p mimics or siNegr1 inhibits the intervention effect of CBD on ferroptosis and the ERK/MEK pathway. Additionally, gene silencing reverses the effect of the miR-320-3p inhibitor on ferroptosis factors in PC12 cells, which suggests that miR-320-3p can target . In conclusion, our findings indicate that CBD can inhibit TBI-induced ferroptosis through the miR-320-3p/Negr1/ERK signaling axis. - Source: PubMed
Publication date: 2026/01/25
Li JialiCao YanLing TenghanLuo XinyuanLi HengxiYin AipingJiang HongyanGuo XiaobingYang LiWu HaiyingLi Ping - Integrated genomic evidence on shared genetic architecture between obesity and psychiatric disorders remains limited. This work utilized multi-level genomic analytic approaches to identify pleiotropic loci, variants, and genes between 14 adiposity traits and 7 psychiatric disorders, including genetic correlation and bidirectional causality as well as gene expression, functional pathway, and druggability, using genome-wide association study data from up to 806,834 individuals of European descent. Based on 67 genetically correlated trait pairs established between the two groups, we identified 17 causal shared genes across 26 tissues, which were enriched in neurodevelopment, neuronal function, cellular transport, and developmental biology. Of these, , , , and were located in the druggable genome, and and were clinically actionable. Mendelian randomization further supported extensive bidirectional causal associations. These findings provide robust evidence for a shared genetic etiology between adiposity and psychiatric disorders, underscoring mechanistic links and prioritizing actionable targets for comorbidity intervention. - Source: PubMed
Publication date: 2026/04/22
Liu DongDou ChunYe ChaojieChen MinglingKong LijieZhu ZhengZheng JieXu MinXu YuLi MianZhao ZhiyunLu JieliChen YuhongYuan ZhongshangNing GuangWang WeiqingBi YufangWang Tiange - Obesity, characterized by abnormal fat accumulation with comorbidities, continues to increase dramatically, particularly in the pediatric population. Identifying the environmental and genetic causes underlying the development of obesity during early childhood is crucial for establishing preventive and protective treatments for this complex disease. We aimed to investigate genetic variants related to non-syndromic early-onset childhood obesity. - Source: PubMed
Publication date: 2026/04/29
Olgun Celebioglu Hazal BanuOzturk Ayse PinarPoyrazoglu SukranTuncer Feyza Nur - Ferroptosis is one of the important mechanisms of secondary neuronal death after spinal cord injury (SCI). However, the upstream regulators that could be targeted for therapeutic intervention remain poorly defined. This study identifies gamma-glutamyl transferase 1 (GGT1) as a key driver of ferroptosis, upregulated in neurons post-SCI. Screening a 150-compound natural product library, we discovered Enocyanin (EA), which reduced GGT1 protein levels, protected neurons from hypoxic injury, and exhibited anti-ferroptotic effects. Mechanistically, EA promoted GGT1 degradation through the E3 ligase MGRN1, leading to K48-linked polyubiquitination and proteasomal clearance, halting ferroptosis. To improve EA's stability and delivery, we engineered a biomimetic nanoplatform (NSCm@EA) using neural stem cell membranes, enhancing drug accumulation at the injured spinal cord. At single-cell resolution, NSCm@EA was shown to precisely remodel neuronal subpopulations, selectively expanding γ-motor neurons and upregulating synaptic genes such as Gria2 and Negr1, while suppressing inflammatory and oxidative stress pathways. In summary, this study reveals GGT1's role in ferroptosis, identifies a natural product that induces its ubiquitin-mediated degradation, and presents a targeted biomimetic delivery strategy for precise intervention in spinal cord injury. - Source: PubMed
Publication date: 2026/05/14
Yang TaoYe LeiXie PeigenSong TaoChen JianZhao HengLiu ZhengshanChen XiDing JianingDing XintianShao AoWu MiaomiaoZhao FengdongTao SiyueYou Tao - Depot-specific fat deposition influences carcass yield and meat quality in ducks. To explore regulatory mechanisms, we profiled adipogenic progenitor cells (APCs) from pectoral muscle (PM), subcutaneous (SAT), and visceral adipose tissue (VAT) using single-cell RNA sequencing. Nine major cell types were identified, with APCs being most abundant in VAT and least abundant in PM, consistent with histological findings. Transcriptomic comparisons revealed depot-specific microenvironments: PM was enriched with myogenic-related pathways, SAT with immune and inflammatory responses, and VAT with pro-adipogenic signaling. Next, APCs were regrouped into 5 subclusters. Cluster 0 (PI16 PDGFRB) enriched in SAT/VAT showed activated signaling of BMP and glycolysis, indicating strong adipogenic potential. Cluster 1 (PDGFRA F3) enriched in PM was associated with Wnt signaling, which maintains APCs in a progenitor state. Cell cycle, RNA velocity, and pseudotime analyses indicated that APCs of SAT/VAT were more advanced in differentiation, while APCs of PM retained stronger proliferative capacity. Cell-cell communication analysis further revealed more active paracrine regulation within SAT/VAT, while APCs from PM showed limited signaling interactions. Key depot-specific regulators were identified, including NEGR1 (PM), CD36 (SAT), and RSPO2 (VAT), which may contribute to regulations of the adipogenic process. This study provides the first single-cell atlas of duck APCs across depots, revealing molecular heterogeneity, lineage dynamics, and niche-specific regulation. These findings advance understanding of depot-specific adipogenesis and offer targets to enhance IMF while limiting excessive SAT and VAT, thereby improving both meat quality and production efficiency. - Source: PubMed
Publication date: 2026/04/23
Wang ZhixiuYang ChunyanLiu SuliJiang YongBai HaoChang GuobinChen GuohongZhao Liang